Tinea corporis is a superficial dermatophyte infection characterized by either inflammatory or noninflammatory lesions on the glabrous skin (ie, skin regions

except the scalp, groin, palms, and soles). Three anamorphic (asexual or imperfect) genera cause dermatophytoses: Trichophyton, Microsporum, andEpidermophyton. Dermatophytes may infect humans (anthropophilic), infect nonhuman mammals (zoophilic), or reside primarily in the soil (geophilic). Dermatophytes preferentially inhabit the nonliving, cornified layers of the skin, hair, and nail, which is attractive for its warm, moist environment conducive to fungal proliferation. Fungi may release keratinases and other enzymes to invade deeper into the stratum corneum, although typically the depth of infection is limited to the epidermis and, at times, its appendages. They generally do not invade deeply, owing to nonspecific host defense mechanisms that can include the activation of serum inhibitory factor, complement, and polymorphonuclear leukocytes. Following the incubation period of 1-3 weeks, dermatophytes invade peripherally in a centrifugal pattern. In response to the infection, the active border has an increased epidermal cell proliferation with resultant scaling. This creates a partial defense by way of shedding the infected skin and leaving new, healthy skin central to the advancing lesion. Elimination of dermatophytes is achieved by cellmediated immunity. Trichophyton rubrum is a common dermatophyte and, because of its cell wall, is resistant to eradication. This protective barrier contains mannan, which may inhibit cell-mediated immunity, hinder the proliferation of keratinocytes, and enhance the organism's resistance to the skin's natural defenses.[1] Tinea corporis is a common infection more often seen in typically hot, humid climates. T rubrum is the most common infectious agent in the world and is the source of 47% of tinea corporis cases.[2, 3] Trichophyton tonsurans is the most common dermatophyte to cause tinea capitis, and people with an anthropophilictinea capitis infection are more likely to develop associated tinea corporis. Therefore, the prevalence of tinea corporis caused by T tonsurans is increasing.[4]Microsporum canis is the third most common causative organism and associated with 14% of tinea corporis infections. A rare case of Microsporum fulvum skin infection (forearm) has recently been reported, identified by ITS sequencing and mass spectrometry.[5] A 5-year study from Kuwait that included 2730 patients reported that fungal skin infections remain prevalent in that country, specifically the Capital area. In those patients with dermatophytes, 6 species were isolated. They

is a fungal infection in hair. Trichophyton violaceum (2. o HIV-positive or immunocompromised patients may develop severe pruritus or pain. often.[7. and Trichophyton verrucosum(0. veterinarian). The history may include occupational (eg.included Trichophyton mentagrophytes (39%). farm worker. o A pruritic. typically caused by T rubrum. Tinea corporis secondary to tinea capitis typically occurs in children because tinea capitis is more common in this population. contact with animals). gardening. contact sports. 8] . laboratory worker. environmental (eg. hair follicles. o Patients can be asymptomatic. the surrounding dermis. o Tinea corporis gladiatorum is a dermatophyte infection spread by skin-to-skin contact between wrestlers.4%). Tinea corporis acquired from animals is more common in children. A few clinical variants are described. Symptoms. T rubrum (10%). with an associated granulomatous reaction. Majocchi granuloma often occurs in females who shave their legs. zookeeper. and.2%). and international residence are relevant clues in the history of a person with tinea corporis. animals. o Majocchi granuloma. contact with sports facilities) exposure. but prevalence is highest in preadolescents. M canis (16%). contact history. annular plaque is characteristic of a symptomatic infection. or inanimate objects. Patients occasionally can experience a burning sensation. but they can greatly affect quality of life. or recreational (eg. Women of childbearing age are more likely to develop tinea corporis as a result of their greater frequency of contact with infected children. recent travel. Age Tinea corporis affects persons of all age groups. with distinct presentations. Sex Tinea corporis occurs in both men and women.    Infected patients may have variable symptoms.[6] Mortality/Morbidity Dermatophyte infections do not result in significant mortality. Tinea corporis may result from contact with infected humans.4%). Epidermophyton floccosum (6.

nonclassic presentation due to corticosteroid treatment. the lesion may become annular in shape.[9] Tinea incognito is tinea corporis with an altered. scaly plaque. papules. Central America.  Following central resolution. Large. crust. called tinea corporis purpurica. tinea corporis can present as purpuric macules. It is caused by Trichophyton concentricum. the South Pacific. vesicles. .o o Tinea imbricata is a form of tinea corporis found mainly in Southeast Asia.[11]  Rarely.  HIV-infected or immunocompromised patients often have atypical presentations including deep abscesses or a disseminated skin infection. Majocchi granuloma manifests as perifollicular. the lesion begins as an erythematous. neck. granulomatous nodules typically in a distinct location. Typically. as shown in the image below. Tinea corporis gladiatorum often manifests on the head. and arms. and even bullae can develop. scaly plaque that may rapidly worsen and enlarge. which is a distribution consistent with the areas of skin-to-skin contact in wrestling.[10]   Tinea corporis can manifest in a variety of ways. especially in the advancing border. as is   shown in the image below. erythematous.  As a result of the inflammation. and South America.[13]  Infections due to zoophilic or geophilic dermatophytes may produce a more intense inflammatory response than those caused by anthropophilic microbes.[12] One report describes 2 cases of tinea corporis purpurica resulting from self-inoculation with Trichophyton violaceum. Annular plaque. which is the lower two thirds of the leg in females. scale.

and fomites (eg hair brushes. if the clinical suspicion is high yet the KOH result is negative. the most common cause is T rubrum.  Tinea imbricata is caused by Trichophyton concentricum. and Microsporum gypseum[9] are also known to produce infection. a geophilic organism.  T verrucosum causes 98% of dermatophyte infections in cattle and is showing increasing prevalence of infection in human contacts. branching hyphae amongst epithelial cells. a fungal culture should be obtained. towels) can spread infection. Because fungal arthroconidia can survive in the environment. although prevalence and patient history are very helpful in identifying the most likely organism. Microsporum canis. such as people.  The KOH helps dissolve the keratin and leaves fungal elements intact. such as chlorazol black E or Parker blue-black ink. A potassium hydroxide (KOH) examination of skin scrapings may be diagnostic in tinea corporis. 14]  T tonsurans. [14]  T mentagrophytes is spread by rabbits. therefore. [15] Trichophyton verrucosum. Trichophyton mentagrophytes.  A counterstain. A few culture mediums are available for dermatophyte growth. may help visualize hyphae under the microscope.       . A KOH preparation from a vesicular lesion should be made from the roof of the vesicle. recurrent outbreaks may occur. Tinea corporis can be caused by a variety of dermatophytes. [10. Trichophyton interdigitale. guinea pigs.  The sample should be taken from the active border of a lesion because this region provides the highest yield of fungal elements.  Infection with M gypseum. can mimic tinea imbricata in presentation.  Infected humans are the most common source of tinea corporis in the United States. Fungal culture is more specific than KOH for detecting a dermatophyte infection.  Contact with contaminated household pets. Dermatophytoses may be acquired from different sources.  Internationally. farm animals. Tinea imbricata is recognized clinically by its distinct scaly plaques arranged in concentric rings.  A KOH test is a microscopic preparation used to visualize fungal elements removed from the skin's stratum corneum. animals. revealing numerous septate. A fungal culture is often used as an adjunct to KOH for diagnosis. or soil. and small rodents.

clotrimazole. potential fungal growth is monitored for 2 weeks. econazole. the molecular method of polymerase chain reaction for fungal DNA identification can be applied. A skin biopsy with a hematoxylin and eosin staining of tinea corporis demonstrates spongiosis. septate branching hyphae are seen in the stratum corneum with hematoxylin and eosin stain.     Sabouraud agar containing neopeptone or polypeptone agar and glucose is often used for fungal culture.  Commonly. sertaconazole) inhibit the enzyme lanosterol 14alpha-demethylase. is similar to Sabouraud agar but has antibiotics. oxiconazole. Gomori methenamine silver) may be required.  DTM contains phenol red solution. Topical therapy is recommended for a localized infection because dermatophytes rarely invade living tissues.  Mycosel. and a superficial inflammatory infiltrate. miconazole. a cytochrome P-450–dependent enzyme that converts lanosterol to ergosterol. gentamicin. If the above clinical evaluations are inconclusive. However. Positive culture results vary depending on the medium used. dermatophyte test medium (DTM) is used. which causes a color change from strawyellow to bright-red under alkaline conditions. On occasion. Topical therapy should be applied to the lesion and at least 2 cm beyond this area once or twice a day for at least 2 weeks. periodic acid-Schiff.[17] Topical azoles and allylamines show high rates of clinical efficacy. However. but special fungal stains (eg. The weakened dermatophyte is . parakeratosis. a major fungal cell membrane sterol. Neutrophils may be seen in the stratum corneum. a commonly used agar. Inhibition of this enzyme results in unstable fungal cell membranes and causes membrane leakage.  The topical azoles (eg. which is a significant diagnostic clue. depending on which agent is used. ketoconazole. Following culture inoculation. chlortetracycline) and antifungal (ie. sulconazole. These agents inhibit the synthesis of ergosterol. This combination isolates dermatophytes while suppressing other fungal and bacterial species that may contaminate the culture. further evaluation for HIV infection and/or an immunocompromised state should be considered.  Sabouraud or Mycosel agar should be used to assess gross and microscopic colony characteristics. indicating a positive dermatophyte culture result. the color makes identification of culture morphology (particularly pigmentation) difficult. it does not contain antibiotics and may allow overgrowth of fungal and bacterial contaminants. cycloheximide) solutions in a nutrient agar base.[16] For atypical presentations of tinea corporis. It contains antibacterial (ie.

With an increased dose of 200 mg/d. terbinafine) and the related benzylamine butenafine inhibit squalene epoxidase.[19] o Oral ketoconazole at 3-4 mg/kg/d may be given. which converts squalene to ergosterol. o Fluconazole at 50-100 mg/d or 150 mg once weekly for 2-4 weeks is used with good results. Liebel et al published in vitro data in 2006.  A low-to-medium potency topical corticosteroid can be added to the topical antifungal regimen to relieve symptoms. It causes membrane instability by accumulating inside fungal cells and interfering with amino acid transport across the fungal cell membrane. the cytochrome P-450 activity of itraconazole allows for potential interactions with other commonly prescribed drugs. naftifine. and telangiectasias. and adverse effects of skin atrophy.[18]  Allylamines (eg. It has fungicidal and antiinflammatory abilities and is used as a broad-spectrum agent. Lastly.000 cases and now is seldom used orally for dermatophyte infections. It may have a reservoir effect and therefore is a good choice for noncompliant patients. resistance to topical antifungal therapy. griseofulvin induces the cytochrome P-450 enzyme system and can increase the metabolism of CYP-450–dependent drugs. immunosuppression. Prolonged use of steroids can lead to persistent and recurrent infections. . Sertaconazole nitrate is one of the newest topical azoles. They also penetrate deeply into hair follicles.   The mechanism of action or oral micronized griseofulvin against dermatophytes is disruption of the microtubule mitotic spindle formation in metaphase. a substance toxic to fungal cells. to accumulate intracellularly and leads to rapid cell death. However.[19]  Ciclopirox olamine is a topical fungicidal agent. the treatment duration can be reduced to 1 week. causing cell membrane destruction. itraconazole. Systemic therapy may be indicated for tinea corporis that includes extensive skin infection. reporting this drug has antiitch properties. longer duration of treatment regimens.unable to reproduce and is slowly killed by fungistatic action. this agent carries an associated risk of hepatitis in less than 1 in 10. Systemic azoles (eg. causing arrest of fungal cell mitosis. fluconazole. striae. In addition. A dose of 10 mg/kg/d for 4 weeks is effective. and comorbidities of tinea capitis or tinea unguium. It is the systemic drug of choice for tinea corporis infections in children. ketoconazole) function similar to the topical agents. but the steroid should only be applied for the first few days of treatment. Inhibition of this enzyme causes squalene. Use of oral agents requires attention to potential drug interactions and monitoring for adverse effects. o Oral itraconazole in doses of 100 mg/d for 2 weeks shows high efficacy. The steroid can provide rapid relief from the inflammatory component of the infection. Allylamines bind effectively to the stratum corneum because of their lipophilic nature. However.

The preferred treatment for tinea imbricata is griseofulvin or terbinafine. Systemic therapy is needed when the infection involves hair follicles. the potential exists for cytochrome P-450.[20] Oral terbinafine may be used at a dosage of 250 mg/d for 2 weeks. such asMajocchi granuloma. topical therapy may serve as adjunct treatment with the oral medication. although some resistance has developed to oral griseofulvin. drug interactions with this agent. In this case. specifically CYP-2D6. voriconazole was the most active and fluconazole was the least active of the azole drugs.o    Based on E-test for susceptibility of T rubrum.[21] .

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